Objectives: The pathogenesis of primary headaches is differential, with a neurogenic inflammation participation.
The aim: The aim of this research was to establish whether inflammation participates in the pathogenesis of migraine and tension-type headaches (ETTH). In order to establish this, the levels of interleukin-6 (IL-6), interleukin-1 beta (IL-1beta), tumor necrosis factor (TNF) and soluble TNF receptor type I (sTNFRI) were detected in groups with headaches during headache-free interval and in controls and in the blood of children with idiopathic headaches to detect changes during headache attack.
Material and methods: 30 children with migraine were included (16 with aura and 14 without aura), 17 boys and 13 girls aged 10-17 years (mean 13.5). The group with ETTH consisted of 31 patients, 24 girls and 7 boys, aged 6-17 years (mean 13.5). The control group, 28 children without headache, diagnosed with non-inflammatory orthopedic diseases, consisted of 15 boys and 13 girls, aged 7-17 years (mean 13.0). When the pain started during hospitalization, the blood was sampled in the first hour of the headache, then 3 hours and 6 hours since headache started (if headache persisted), and 6 hours after its termination. Two days after the pain termination, the blood samples were collected in children suffering from headaches, as the headache-free measurements and in controls under the same conditions at 7 a.m. after awakening. The cytokine level was established using Biosource kits, all 326 samples were processed. The statistical assessment was conducted.
Results: No differences were detected in cytokine levels between the groups with migraine and ETTH and with comparison to controls during headache-free interval and during headache attack as well. However, it was established that in 12/30 children with migraine there was a significant increase in IL-6 level in the first hour of the migraine attack. This group consisted of 12 children with TNF level higher and the tendency toward decrease in sTNFRI was established, 3 hours since headache started, as compared to 18/30 children with migraine but without increase in IL-6. The correlation between the level of cytokines and age and weight was not detected. Also no correlation was established between cytokine levels and leukocyte and thrombocyte count.
Conclusion: 1. Changes of the level of IL-6, IL-1beta, TNF and sTNFRI in the blood of children with idiopathic headache do not indicate a significant role of inflammatory process in its pathogenesis. 2. Although the significant increase in IL-6 levels observed in several children in the first hour of the migraine attack may suggest that neurogenic inflammation participates in the pathogenesis of migraine.